carbon monoxide

carbon monoxide is a gas which is best known to us as a product of incomplete combustion. As such, mankind must have been aware of its deadly effect since the discovery and use of fire, and increasingly so as the development of the industrial revolution led to more use of combustion as a source of energy. The important producers of carbon monoxide are industrial processes, heating equipment, accidental fire, cigarettes, and the internal combustion engine. Blast furnace gas contains 25% carbon monoxide, and coal gas, which was used as a fuel in Europe up until North Sea (natural) gas became plentiful, contains 16%. Carbon monoxide poisoning is the most common cause of fatal gassing and is the cause of death in about 90% of fire victims. Domestic gas supplies still lead to carbon monoxide poisoning, but now due to leakage of products of combustion from a damaged flue or poorly maintained equipment, rather than the fuel itself, since natural gas is carbon monoxide free. In the mining industry carbon monoxide contaminates the atmosphere during and after fires or explosions. The ‘afterdamp’ occurring in such situations is a mixture of carbon dioxide and carbon monoxide.

Carbon monoxide is a colourless, odourless gas which is tasteless and non-irritant. It is somewhat less dense than air and, although it is a product of imperfect combustion, it is inflammable. The gas was first identified by Joseph Priestley in the eighteenth century, but it was Claude Bernard in 1870 who discovered the affinity between carbon monoxide and haemoglobin which accounts for its deadliness: carboxyhaemoglobin is formed and oxygen transport from the lungs to the tissues disrupted. In 1895 J. S. Haldane demonstrated that the formation of carboxyhaemoglobin is an equilibrium reaction which depends upon the relative partial pressures of carbon monoxide and oxygen in inspired gas. Haldane's interest was stimulated by the problems caused by carbon monoxide in British coal mines. By breathing carbon monoxide gas which was passed through a bottle containing a mouse, he was able to determine that man was very much more resistant to the gas. Small animals such as mice and canaries, who are more vulnerable than man due to their high metabolic rate, were used in mines to give an indication of carbon monoxide contamination. Canaries responded to the gas by falling off their perches before workers noticed any ill effects, and this normally gave ample warning. Occasionally, however, in low concentrations of the order of 0.05% carbon monoxide, the bird adapted to the gas and the workers could collapse while the bird remained well.

Carbon monoxide, like oxygen, has an affinity for iron-containing molecules, but it is about 210 times more effective in binding to iron-containing haemoglobin than oxygen is. Since air contains 21% oxygen this means that only 0.1% carbon monoxide in the air will eventually lead to 50% of the haemoglobin being combined to form carboxyhaemoglobin. Once carboxyhaemoglobin is formed, and after exposure ceases, it takes 4–5 hours for its level in the blood to fall, exponentially, by 50%. The ill effect of the gas can therefore be cumulative, and a person can be poisoned by intermittent exposure during the day.

Because carboxyhaemoglobin does not carry oxygen, a level of 50% means that the oxygen carrying capacity of the blood is reduced by 50% and there is a corresponding reduction in the ability to perform maximum exercise. The body compensates for the blood's reduction in oxygen carrying capacity by increasing cardiac output, and in the early stages of carbon monoxide poisoning the heart beats faster and more strongly. Unfortunately, haemoglobin is not the only molecule affected. Muscle myoglobin also binds carbon monoxide, 60 times more effectively than it binds oxygen. This results in a reduction of heart muscle contractility and a failure of the body's compensatory mechanisms, leading to profound tissue hypoxia, which can be fatal. The presence of carboxyhaemoglobin also diminishes the oxygen held by the normal haemoglobin, which further compounds the hypoxic effect. As tissue oxygen level falls, carbon monoxide is able to bind to other iron-containing molecules: notably cytochrome P450, an important drug-metabolizing enzyme, and cytochrome A3, an enzyme in the terminal respiratory chain which can also be poisoned by cyanide.

The scientific history of carbon monoxide is not one of uniform gloom, however. The intense affinity of carbon monoxide for haemoglobin has allowed low concentrations to be used as a marker for measurement of the speed of blood through the lungs and the surface area of the lung available for the transfer of oxygen. This latter remains as one of the standard lung function tests. In 1951 Sjöstrand discovered that Haldane's poison gas is a normal product of the body's metabolism. The enzyme haem oxygenase breaks down the haem from senescent red blood cells, and this reaction produces carbon monoxide and bile salts. The bile salts are excreted by the liver and the carbon monoxide released gives the blood a normal carboxyhaemoglobin level of 0.2–1.0%. This endogenous carbon monoxide was thought to be just a waste product, but more recent work by Verma has demonstrated that a type of haem oxygenase is located in specific areas in the brain, and suggested that the carbon monoxide produced acts as a neurotransmitter. The carbon monoxide activates the enzyme guanylyl cyclase, as does nitric oxide, regulating the intracellular levels of the second messenger cyclic GMP, which in turn regulates cellular activity. Other workers have demonstrated the haem oxygenase enzyme system in blood vessel walls and demonstrated that the carbon monoxide released causes vasodilation, as does nitric oxide. So far, endogenous carbon monoxide release has been suggested to have a role in the sense of smell, memory, cerebellar function (and hence the body's balance and co-ordination), control of blood hormone levels from the hypothalamus, and control of smooth muscle tone and vasodilatation.

The symptoms of carbon monoxide poisoning depend on the concentration breathed. The victim may pass out without warning, but often the onset of poisoning is slow. Headache, with or without nausea, is common, and this may relate to carbon monoxide's vasodilating effect. Drowsiness and lethargy then occur, along with breathlessness on exertion. At any stage there may be chest pain; this is angina due to cardiac hypoxia. At the stage of lethargy and drowsiness, cerebral function is affected and the person may not be able to think well enough to make an escape effort. Coma follows, and death. Treatment is by removal to an uncontaminated atmosphere and the administration of 100% oxygen. Hyperbaric oxygen speeds up recovery, and there is increasing evidence that it reduces long-term neurological problems.

Endogenous carbon monoxide function is undoubtedly disrupted during poisoning, but at our present state of knowledge it is difficult to say how this contributes to the toxic action of exogenous carbon monoxide. It may well be that our picture of the mechanisms of carbon monoxide poisoning will change as the function of endogenous carbon monoxide becomes clearer. Patients with carbon monoxide poisoning may have very poor balance and yet have good cerebral function. Short-term memory may also be severely disrupted. It is tempting to link these two features with the functions suggested for endogenous carbon monoxide. No doubt time will tell if there is a relationship.

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Carbon Monoxide

UXL Encyclopedia of Science
COPYRIGHT 2002 The Gale Group, Inc.

Carbon monoxide

Carbon monoxide is a compound of carbon and oxygen in which the ratio of the two elements is one atom of carbon to one atom of oxygen. Its formula is CO. Carbon monoxide is a colorless, odorless, tasteless, poisonous gas. Most people have heard about carbon monoxide because of its toxic effects. People who live or work in crowded urban areas may become ill with headaches and nausea because of exposure to carbon monoxide in polluted air. In higher concentrations, the gas can even cause death.

History

The early history of gases such as carbon monoxide is sometimes difficult to trace. Until the early 1600s, scientists did not realize that the material we call air is actually a mixture of gases. As early as the late thirteenth century, Spanish alchemist Arnold of Villanova (c. 1235–1311) described a poisonous gas formed by the burning of wood; this gas was almost certainly carbon monoxide.

Flemish scientist Jan Baptista van Helmont (c. 1580–1644; some sources give death date as 1635) nearly died as a result of inhaling gas carbonum, apparently a mixture of carbon monoxide and carbon dioxide. Credit for the discovery of carbon monoxide, however, is usually given to English chemist and theologian Joseph Priestley (1733–1804). During the period between 1772 and 1799, Priestley gradually recognized the difference between carbon dioxide and carbon monoxide and correctly stated the properties of the latter gas.

Sources

Like carbon dioxide, carbon monoxide is formed naturally during the combustion (burning) of wood, coal, and other naturally occurring substances. Huge quantities of carbon monoxide are produced, for example, during a forest fire or a volcanic eruption.

Words to Know

Combustion: Oxidation that occurs so rapidly that noticeable heat and light are produced; burning.

Hemoglobin: An complex iron-containing molecule that transports oxygen through the circulatory system.

Incomplete combustion: Combustion that occurs in such a way that fuel is not completely oxidized ("burned up"). The incomplete combustion of carbon-containing fuels (such as coal and oil) always results in the formation of some carbon monoxide.

Reducing agent: A substance that removes oxygen from some other material.

Toxic: Poisonous.

The relative amounts of carbon monoxide or carbon dioxide that form during combustion depend on two factors: the amount of oxygen present and the combustion temperature. When a large supply of oxygen is present and when the combustion temperature is high, carbon dioxide is more likely to be formed. With limited supplies of oxygen and at lower temperatures, carbon monoxide is produced.

Carbon monoxide is not extracted from the air very easily but is produced commercially by the controlled oxidation of carbon. For example, producer gas is a product made by blowing air across very hot coke (nearly pure carbon). Producer gas consists of three gases: carbon monoxide, carbon dioxide, and nitrogen in the ratio of 6 to 1 to 18. Water gas is made by a similar process—passing steam over hot coke. The products in this case are hydrogen, carbon monoxide, carbon dioxide, and other gases in the ration of 10 to 8 to 1 to 1.

Physiological effects

The poisonous character of carbon monoxide has been well known for many centuries. At low concentrations, carbon monoxide may cause nausea, vomiting, restlessness, and euphoria (a feeling of well-being). As exposure increases, a person may lose consciousness and go into convulsions. Death is a common final result. The U.S. Occupational Safety and Health Administration has established a limit of 35 parts per million of carbon monoxide in workplaces where a person may be continually exposed to the gas.

Scientists now know how carbon monoxide poisoning occurs. Normally, oxygen is transported from the lungs to cells by means of red blood cells. This process occurs when oxygen atoms bond to an iron atom in the middle of a complex molecule known as oxyhemoglobin. Oxyhemoglobin is a fairly unstable molecule that breaks down to release free oxygen and hemoglobin for use by the body's cells. The oxygen is then available to carry out reactions in cells from which the body gets energy.

If carbon monoxide is present in the lungs, this sequence of reactions is disrupted. Carbon monoxide bonds with iron in hemoglobin to form carbonmonoxyhemoglobin, a complex somewhat similar to oxyhemoglobin. Carbonmonoxyhemoglobin, however, is a more stable compound than oxyhemoglobin. When it reaches cells, it has little tendency to break apart; instead, it continues to circulate in the bloodstream in its bound form. As a result, cells are unable to obtain the oxygen they need for energy production, and the symptoms of carbon monoxide poisoning begin to appear.

Carbon monoxide poisoning—at least at moderate levels—is so common in everyday life that carbon monoxide detectors, similar to smoke alarms, are found in many businesses and homes. Poorly ventilated charcoal fires, improperly installed gas appliances, and exhaust from automobiles and trucks are the most common sources of the gas. In fact, levels of carbon monoxide in the air can become dangerously high in busy urban areas that have large numbers of cars and trucks. Cigarette smokers may also be exposed to harmful levels of the gas. Studies have shown that the one-to-two pack-a-day smoker may have up to 7 percent of the hemoglobin in her or his body tied up in the form of carbonmonoxyhemoglobin.

Uses

Carbon monoxide is used in industry primarily as a source of energy and as a reducing agent. Both producer and water gas are burned as fuels for a variety of industrial operations. As a reducing agent, carbon monoxide is used to convert the naturally occurring oxide of a metal to the pure metal. When carbon monoxide is passed over hot iron oxides, for example, the oxides are converted to metallic iron.

[See alsoCarbon dioxide; Carbon family ]

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Carbon Monoxide

Encyclopedia of Public Health
COPYRIGHT 2002 The Gale Group Inc.

CARBON MONOXIDE

Carbon monoxide (CO) is a clear, colorless, odorless, and insidious poison that is responsible for hundreds of inadvertent and preventable deaths in the United States each year. The major environmental source of CO is incomplete combustion of carbonaceous fossil fuels. The reason for its toxicity is that it combines with the oxygen-carrying site of hemoglobin, the red protein within red blood cells that is responsible for delivering oxygen from the lung to body tissues. CO has a more than two-hundredfold greater affinity for this oxygen-carrying site than does oxygen. This means that, at sea level, exposure to 1,000 parts per million (ppm) CO in 20 percent oxygen (200,000 ppm) would lead, at equilibrium, to about 50 percent of hemoglobin sites being combined with CO rather than oxygen. Fortunately, it requires eight to twelve hours for maximum blood levels to be achieved when the body encounters a new CO concentration, otherwise mainstream cigarette smoke, which contains even higher levels of CO, might be instantaneously lethal. When CO combines with hemoglobin, the resulting chemical is called carboxy hemoglobin (COHb).

The negative effect of CO on the delivery of oxygen to the tissues extends beyond just the simple blockage of oxygen-combining sites. Each hemoglobin molecule contains four oxygen-carrying sites. Once the first oxygen molecule is released at the tissue level the second, third, and fourth come off even more rapidly. Oxygen release is delayed by CO so that there is even less oxygen delivered than would be expected purely on the basis of the amount of oxygen not being carried by hemoglobin. For this reason, overt symptoms due to lack of oxygen can be observed at COHb levels of approximately 15 to 20 percent, or even less, in healthy people. Levels of COHb over 40 percent can be lethal.

The uptake of CO increases as respiratory rates increase. This puts children at greater risk since they breathe more rapidly, in proportion to their body weight, than adults. This explains the unfortunate situation of a family in an automobile stuck in a snowstorm with the motor running being found with the adults unconscious and the children dead. The fetus is also at higher risk due to the greater affinity of CO for fetal, as compared to adult, hemoglobin.

All cases of fatal CO poisoning are readily preventable. In addition to automobile exhaust, other lethal sources of CO are often related to home heating systems. Blockage of flues, or inappropriate repair work on the home heating source or on ducts, is often responsible for CO toxicity. Symptoms of CO toxicity, such as headache, weakness, and listlessness, tend to be worse in the morning and to go away during the day if people leave the home. Many fatal cases are preceded by visits to physicians or emergency departments with only symptomatic treatment. Home CO alarms are relatively cheap and are an effective means of prevention. CO poisoning occurs more rapidly at high altitude due to the relative lack of oxygen to compete for the oxygen-combining site of hemoglobin. Conversely, symptomatic CO poisoning is treated with oxygen.

CO is also made in the human body through the normal catabolism of heme (oxygen-carrying hemoglobin), which leads to a background concentration in the blood of approximately 0.5 percent COHb. Concentrations of 2 to 3 percent COHb have been associated with an increased risk of angina attacks in susceptible individuals with preexisting arteriosclerotic heart disease. Preventing this adverse consequence is the major basis for the current U.S. ambient standard for CO. There has been a significant decline in outdoor CO levels in the United States as a result of decreased automotive emissions of carbon monoxide.

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Carbon Monoxide

Pollution A to Z
COPYRIGHT 2004 The Gale Group Inc.

Carbon Monoxide

Carbon monoxide is an invisible, odorless, and poisonous gas with the chemical formula CO. Because of its toxicity, the U.S. Environmental Protection Agency (EPA) regulates CO. The gas is a by-product of incomplete combustion (burning with insufficient oxygen). Its major source is vehicle exhaust (60 percent). Other sources include water heaters and furnaces, gas-powered
engines (boats and lawn mowers), charcoal and wood fires, agricultural burning, and tobacco smoke.

CO is classified as an indirect greenhouse gas. It does not contribute to global warming directly, but leads to the formation of ozone. Ozone is the major air pollutant formed in photochemical smog and a potent greenhouse gas.

Human exposure to elevated CO impairs oxygen uptake in the bloodstream. Under CO-free conditions, oxygen is transported from the lungs to tissues by hemoglobin. When CO is present, it mimics the shape of oxygen and binds instead to the hemoglobin. The molecule is not easily released, blocking further oxygen uptake, and ultimately depriving organs and tissues of life-sustaining oxygen. The symptoms of CO poisoning range from dizziness, mild headaches, and nausea at lower levels to severe headaches, seizures, and death at higher levels.

The EPA national outdoor air quality standard for CO is nine parts per million or ppm (0.0009 percent) averaged over an eight-hour period. The gas is life-threatening after three hours at 400 ppm (0.04 percent) and within minutes at 1.28 percent. In 1996, 525 deaths in the United States were attributed to unintentional and 1,988 deaths to intentional CO poisoning.

Exposure to CO can be reduced by assuring adequate ventilation when near any combustion source. Indoor cooking with charcoal and running gaspowered engines inside a garage are both dangerous and should be avoided. Fuel-burning appliances and fireplaces ought to be routinely inspected.

CO detectors are available to detect less obvious sources, such as a malfunctioning furnace. The sensors operate in one of three ways: They mimic the body's response to CO (biomimetic detectors), they allow a heated metal oxide to react with the gas (metal oxide detectors), or they facilitate a reaction using platinum electrodes immersed in an electrolyte solution (electrochemical detectors). The lowest level that a CO alarm can detect is 70 ppm.

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carbon monoxide

The Columbia Encyclopedia, 6th ed.

Copyright The Columbia University Press

carbon monoxide, chemical compound, CO, a colorless, odorless, tasteless, extremely poisonous gas that is less dense than air under ordinary conditions. It is very slightly soluble in water and burns in air with a characteristic blue flame, producing carbon dioxide; it is a component of producer gas and water gas, which are widely used artificial fuels. At high pressures and elevated temperatures it reacts with hydrogen in the presence of a catalyst to form methanol, and under similar conditions reacts with methanol to produce acetic acid. It is also used in the production of polycarbonate and polyurethane as well as detergents. As a reducing agent, removing oxygen from many compounds, it is used in the reduction of metals, e.g., iron (see blast furnace), from their ores.

Carbon monoxide is formed by combustion of carbon in oxygen at high temperatures when there is an excess of carbon. It is also formed (with oxygen) by decomposition of carbon dioxide at very high temperatures (above 2,000°C). It is present in the exhaust of internal-combustion engines (e.g., in automobiles) and is generated in coal stoves, furnaces, and gas appliances that do not get enough air (because of a faulty draft or for other reasons).

Carbon monoxide is an extremely poisonous gas. Breathing air that contains as little as 0.1% carbon monoxide by volume can be fatal; a concentration of about 1% can cause death within a few minutes. The gas is especially dangerous because it is not easily detected by human senses. Early symptoms of carbon monoxide poisoning include drowsiness and headache, followed by unconsciousness, respiratory failure, and death. First aid for a victim of carbon monoxide poisoning requires access to fresh air; administration of artificial respiration and, if available, oxygen; and, as soon as possible, expert medical attention. When carbon monoxide is inhaled, it reacts with hemoglobin, the red blood pigment that normally carries oxygen to all parts of the body. Because carbon monoxide is attracted to the hemoglobin about 210 times as strongly as is oxygen, it takes the place of oxygen in the blood, causing oxygen starvation throughout the body. Carbon monoxide detectors for homes are now readily available.

Carbon monoxide from automobile and industrial emissions is a dangerous pollutant that may contribute to the greenhouse effect and global warming. In urban areas carbon monoxide, along with aldehydes, react photochemically to produce peroxy radicals. Peroxy radicals react with nitrogen oxide to increase the ratio of NO2 to NO, which reduces the quantity of NO that is available to react with ozone (see smog). Carbon monoxide is also a constituent of tobacco smoke.

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carbon monoxide

carbon monoxide Colourless, odourless poisonous gas (CO) formed during the incomplete combustion of fossil fuels, occurring for example in coal gas and the exhaust fumes of cars. Carbon monoxide poisons by combining with the haemoglobin in red blood cells and thus preventing them from carrying oxygen around the body. (This happens if the inhaled air contains only 0.1% of carbon monoxide by volume.) It is used as a reducing agent in metallurgy. Properties: density 0.968 (air = 1); m.p. −205°C (−337°F); b.p. −191.5°C (−312.7°F).

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carbon monoxide

carbon monoxide A colourless odourless gas, CO. It is formed by the incomplete combustion of carbon and is present in car-exhaust gases. Carbon monoxide is able to bond with metals; this accounts for its toxicity, which is due to the binding of the CO to the iron in haemoglobin, thereby blocking the uptake of oxygen. See carboxyhaemoglobin.

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carbon monoxide

carbon monoxide (mŏn-ok-syd) n. a colourless almost odourless gas that is very poisonous. When breathed in it combines with haemoglobin in the red blood cells (see carboxyhaemoglobin). Carbon monoxide is present in coal gas and motor exhaust fumes. Formula: CO.

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